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DNFB
1-fluoro-2,4-dinitro-benzene

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This biphasic pattern of ear swelling seen in IgE-sensitized mice was temporally indistinguishable from that observed in mice conventionally sensitized for allergic contact dermatitis reactions by epicutaneous application of DNFB 5 days before DNFB ear challenge [4].

Both C3-modulated systems totally reversed the failure to induce a contact sensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization at the UV-exposed site, as well as immunologic tolerance to a second DNFB immunization through normal skin [7].

After challenge with 0.1% DNFB, IL-10-treated mice showed an ear swelling response (delta mm-2 = 13 +/- 3; group 1) similar to that of control mice only sensitized with DNFB (delta mm-2 = 14 +/- 3; group 3) [8].

We have presented data showing that IFN-beta at 1,000 U/mouse i.v. inhibits the generation of Ts-mediated tolerance to dinitrofluorobenzene (DNFB) and abrogates the transfer of suppression by Ts [9].

Tolerance to DNFB-RBC was highly specific in vivo; mice tolerant to DNFB showed normal reactivity to TNCB (picryl chloride.) Cells of mice tolerant to DNFB-RBC were also unresponsive to DNBSO3 in vitro[28].

To determine whether UVB can induce suppression in TNF-R1(-) mice, mice were irradiated on the shaved abdomen with 96 mj/cm2 UVB and 3 days later they were painted with 0.5% DNFB (sensitization dose), followed 5 days later with 0.2% DNFB to the left ear (challenge dose) [30].

Significant increases in IL-2 mRNA were detected in the skin after dinitrofluorobenzene challenge in normal mice, while this response was blunted in CD28 -/- mice [31].

In contrast, following challenge with DNFB, expression of B7-2 is up-regulated in both epidermis and dermis[33].

Local injection of IL-1ra to sensitized BALB/c mice just before challenge with dinitrofluorobenzene resulted in a significant reduction in the intensity of CHS responses, assessed by ear swelling [34].